1/5 Answer: Koroneiki is one of the highest in polyphenols in general. The other 3 highest are Cornicabra, Coratina, Moraiolo
A brief primer on olive oil (OO): 1- green color is due to higher content of chlorophyll A and B, yellow is due to carotenoids. Green = earlier harvest
2/5 2- OO contains 55-83% oleic acid, 18 carbons, 1 double bond (18:1, monounsaturated). 3- The rest is saturated(<5%) and 18:2 fatty acids (<20%). If there more than ~1% 18:3, it means its adulterated - mixed with other oils and is fake. This is detected by chemical analysis
3/5 4- extra virgin OO has low 'acid' content (<0.8%), i.e. free fatty acids (FFA) broken down from the triglyceride. Ideally should be pressed by 24 hours after picking, but the FFA is key
5- should be very low in peroxides (pro-oxidant, rancidness) - i.e not exposed to O2
4/5 6- polyphenol conc can be as high as 3-500 mg/kg. agbiolab.com/files/agbiolab… The earlier olives are picked the more polyphenols/anti-oxidants they conation.
5/5 We went to Greece, drew blood from villagers, brought it to US and showed for same LDL-C, LDL was enriched in oleic acid, highly resistant to oxidation and had less monocyte activity- an early benefit against atherosclerosis and of Med Diet
I hope everyone enjoyed this part
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1/8 this topic needs a few comments: 1- The Mediterranean diet does have more fat than AHA recommends, but its mainly in olive oil. Taking into account the usual limitations of diet studies, Mediterranean diets do reduce CVD events, nejm.org/doi/full/10.10…
1/2 2- The AHA has done an admirable job in public health in advocating low LDL-C, this led to all stakeholders getting it down, and taking into account that average LDL-C has slowly gone down in US, it likely has saved hundreds of thousands in not millions of lives.
1/3 3- the AHA did not emphasize caloric restriction enough along with reducing fat, so people felt they could eat as much as they wanted to as long as it was not fat. It goes to my earlier point, when you take away something, somehting else fills the void- 2 variables changing
and 12-19:
12/19- 5.In another study healthy women were fed two diets containing a reduced amount of total and saturated fat, with either low or high in vegetables, berries, and fruit. While LDL-C declined, Lp(a) increased 7-9% ncbi.nlm.nih.gov/pubmed/14739118
13/19- 6.Weight loss also tends to increase Lp(a), particularly in patients with small isoforms. ncbi.nlm.nih.gov/pmc/articles/P…
14/19-7.On the other hand, plant based diets seem to lower Lp(a) and all atherogenic lipoproteins. ncbi.nlm.nih.gov/pubmed/30014498
1/19 1/x Let’s start with the basics- what are the different types of fats: saturated, monounsaturated and polyunsaturated. These are defined by the # of carbon-carbon double bonds of the fatty acids that are amenable to reactions.
2/19 In terms of effects on LDL-C, excessive intake of saturated fats raises LDL-C and mono and poly are neutral or lower LDL-C. This has to do mainly with how the fats interact with genes in the liver to affect LDL metabolism.
3/19 On other hand, the opposite occurs with oxidation: sat fats cannot be oxidized, mono are difficult to oxidize, and poly are very easy to oxidize. For a simple and superficial explanation, oxidation is the addition of oxygen to the fatty acid at the site of the double bonds,
1/21 Saturday Morning Class #8 Lp(a) and niacin @OxPL_apoB
Basics: What is niacin?. It is vitamin B3 (i.e. essential nutrient) that is precursor of coenzymes NAD+ and NADP+, which shuttle around protons and electrons to mediate redox reactions for fat, carb, protein metabolism
2/21 How does niacin affect the lipid panel: at 2 gram/day: Lp(a) down 25%, LDL-C down 16%, TG down 32%, HDL up 24%. All modest, but going in right direction.
3/21 6 trials done pre 1998, some outcomes, some angiography, all tended to show benefit. Most were combo with clofibrate, colestipol, prava, lova or gemfibrozil. Also other arms with different Rx. However only one with niacin monotherapy - Coronary Drug Project published 1975
Let’s define what Lp(a) is: 2 major proteins stuck together like conjoined twins, apolipoprotein(a) and apolipoprotein B-100. The ratio of each is 1:1- if you know how much apoB is on Lp(a) then you know how much apo(a) is on it
2/17 ApoB-100 is a lipoprotein, it has a specific folded structure that can allow it to be loaded with lipid molecules, which don’t dissolve in water, so that these can be sent throughout the body for various needs- precursor to hormones, adrenal metabolites, cell membranes, etc.
3/17 Think of apoB-100 as pack mules that can load and offload cargo- VLDL, LDL, IDL, small dense LDL, OxLDL and OxPL
Apo(a) is not lipoprotein, so when its on apoB-100 it sticks out in the liquid phase of blood, think of it like a pool sweeper
When one looks at your lab report, note the LDL-C says “calculated”. So, believe it or not, the most important risk factor for CVD is actually an estimated value. Hard to believe but true. 1/17
Sometimes it says direct LDL, which is an actual measurement. LDL is a complex particle containing apoB, cholesterol, cholesteryl esters, phospholipids and a bit of triglyceride. LDL-C only reflects the total cholesterol in LDL, that is why there is a “C” at end of it. 2/17
LDL particles are made of about 50% cholesterol by mass (i.e. the human body is 60% water). Lp(a) on other hand is 20-45% cholesterol. The gold standard for measuring LDL-C is ultracentrifugation. 3/17